Executive Neurocognition Memory Systems

Clinical Psychology Review 26 (2006) 346 – 375
Executive neurocognition, memory systems,

and borderline personality disorder
Eric A. Fertuck a,T, Mark F. Lenzenweger c, John F. Clarkin d,
Simone Hoermann e, Barbara Stanley a,b
a
New York State Psychiatric Institute, Columbia University, College of Physicians and Surgeons, United States
b
John Jay College, City University of New York, United States
c
State University of New York at Binghamton, United States
d
Weill Medical College of Cornell University, United States
e
Columbia University Medical Center, United States
Received 13 April 2004; accepted 9 May 2005
Abstract
Borderline Personality Disorder (BPD) is a common, disabling, and burdensome psychiatric condition. It is
characterized by turbulent fluctuations of negative emotions and moods, unstable and conflictual interpersonal
relationships, an incoherent and often contradictory sense of self, and impulsive, potentially lethal self-injurious
behaviors. The neurobehavioral facets of BPD have not been extensively studied. However, clinical theoreticians
and researchers have proposed that the symptoms and behaviors of BPD are, in part, associated with disruptions
in basic neurocognitive processes. This review summarizes and evaluates research that has investigated the
relationship between executive neurocognition, memory systems, and BPD. Three historical phases of research
are delineated and reviewed, and the methodological and conceptual challenges this body of investigation
highlights are discussed. Laboratory-based assessment of executive neurocognition and memory systems is
integral to an interdisciplinary approach to research in BPD. Such an approach holds promise in elucidating the
T Corresponding author. Tel.: +1 212 543 6926; fax: +1 212 543 6946.
E-mail address: ef304@columbia.edu (E.A. Fertuck).
0272-7358/$ - see front matter D 2005 Elsevier Ltd. All rights reserved.
doi:10.1016/j.cpr.2005.05.008
E.A. Fertuck et al. / Clinical Psychology Review 26 (2006) 346–375 347
neurobehavioral facets, development, diagnostic boundaries, prevention, and optimal interventions for this
debilitating and enigmatic disorder.
D 2005 Elsevier Ltd. All rights reserved.
Keywords: Borderline personality; Memory systems; Memory; Cognition; Executive function; Neurocognition; Neuropsy-
chology; Neuroscience
Borderline personality disorder (BPD; Diagnostic and Statistical Manual, 4th Edition; DSM-IV;
American Psychiatric Association, 1994) is characterized by turbulent, anxious, angry, and depressive
emotional states, unstable interpersonal relationships, an incoherent and often contradictory self-concept,
and impulsive and often dangerous behaviors such as self-injury and drug abuse. Following the
pioneering clinical descriptions of borderline personality (Grinker, Werble, & Drye, 1968; Kernberg,
1967), empirical research of BPD has progressed over the last 20 years. Based on recent population
prevalence estimates (0.3–0.7%), between six-hundred thousand and 1.4 million adults in the United
States meet diagnostic criteria for BPD (Lenzenweger, Loranger, Korfine, & Neff, 1997; Samuels et al.,
2002; Torgersen, Kringlen, & Cramer, 2001). The suicide rate for BPD individuals is about 10% (Paris,
2002; Stone, 1993), comparable to the other psychiatric disorders such as schizophrenia and major
depression. In addition, 69% to 75% of individuals with BPD engage in self-injurious behaviors (Clarkin,
Widiger, Frances, Hurt, & Gilmore, 1983; Cowdry, Pickar, & Davies, 1985), and the frequency of self-
injurious behaviors is more than in any other psychiatric diagnosis (Stanley, Winchel, Molcho, Simeon, &
Stanley, 1992). Individuals with BPD exhibit high drop out rates and variable improvement in
psychotherapy (Clarkin, 1996), and respond only partially to psychopharmacological therapies (Soloff,
2000). Additionally, this diagnostic group utilizes health care services more frequently than any other
psychiatric group (Bender et al., 2001). Despite this troubling clinical picture, BPD has not received
research attention and widespread clinical focus commensurate with the suffering and mortality it causes.
There is considerable reason to suspect that there are disruptions in basic executive neurocognition
and memory processes in BPD. Central to the symptoms of BPD is unstable and dysregulated inhibitory
control over behavior, emotion, and cognition. The acquisition of executive neurocognition is
inextricably linked to emotion and personality development, and inhibitory capacity influences the
acquisition of prosocial behaviors, affect regulation, and problem solving abilities (Derryberry & Reed,
1994; Posner & Rothbart, 2000). These capacities are commonly impaired in BPD. From a clinical
perspective, neurocognitive function predicts response to intervention in other clinical groups (e.g.,
Smith, Hull, Romanelli, Fertuck, & Weiss, 1999). Should BPD individuals, or subgroups of them,
evidence a characteristic constellation of inhibitory and memory characteristics, treatment could be
tailored to complement them, leading to improved treatment planning and interventions. From a
scientific vantage point, BPD is a diagnostic entity that can be used to elaborate the understanding of
basic cognitive and affective processes. The study of emotion, mood, temperament, affect regulation,
and their relationship with personality, cognition, and psychopathology are at the center of rapid,
exciting developments in cognitive (Gazzaniga, 2000) and affective science (Davidson, Scherer, &
Goldsmith, 2003).
Previous reviews have emphasized the clinical implications of neurocognitive functioning in BPD and
other personality disorders (see Gorton, Swirsky-Sacchetti, Sobel, Samuel, & Gordon, 1999; O’Leary &
Cowdry, 1994). This review, by contrast, focuses on research that has attempted to systematically
348 E.A. Fertuck et al. / Clinical Psychology Review 26 (2006) 346–375
characterize executive neurocognition and memory systems in BPD. First, we define the types and
subtypes of executive neurocognition and memory of relevance to BPD. A historical review of three
phases of research in executive neurocognition, memory, and BPD follows. Finally, then we discuss the
literature in this area as it relates to the neurobiology and neuroscience, development, and clinical
understanding BPD.
1. Memory systems and cognitive inhibition: domains and methodologies
1.1. Memory systems
Memory can be organized into five distinct systems (see Schacter, Wagner, & Buckner, 2000 for
review): working memory, semantic memory, episodic memory, the perceptual representational system,
and procedural memory. Studies of BPD to date have almost exclusively focused on working memory,
semantic memory, and, to a lesser extent, episodic memory in BPD.
Working memory involves the conscious storage and manipulation of mental representations. It
involves a tripartite set of functions, a central executive system, and the phonological loop and visuo-
spatial subsystems. Brain imaging studies have implicated the activation of the left inferior prefrontal,
dorsolateral prefrontal, supplementary motor, premotor, posterior–parietal, and cerebellar cortices in
verbal working memory. In comparison, the posterior, inferior prefrontal, premotor and dorsolateral
prefrontal cortices have been observed in spatial working memory. The central executive system
consistently involves the dorsolateral prefrontal cortex, in particular for more complex tasks (Baddeley,
1998; Schacter et al., 2000).
Episodic, or, autobiographical memory is the recollection of periods from personal history that
involve the encoding of the specifics of time, context, and place. The encoding of such memories
involves the left inferior prefrontal cortex and the anterior medial temporal lobe, including the
hippocampus. Retrieval of episodic memories involves both the right anterior prefrontal cortex and the
medial parietal cortex (Schacter et al., 2000).
Finally, procedural memory involves storage of behavioral, motoric, affective, and cognitive skills
and habits. Even with damage to medial temporal lobe structures, the acquisition of procedural skills is
not affected, indicating the functional dissimilarity between procedural and other forms of memory. As
procedural tasks that are just being learned become automatized over time, there is a transition from the
use of prefrontal and premotor activation to more non-deliberative neural pathways (Schacter et al.,
2000).
1.2. Executive neurocognition
Executive neurocognition involves the delay or termination of a cognitive or motor response in order
to achieve a less immediate goal or reward. Executive neurocognitive controls are relevant to
psychopathology research, as impairments in such functions are implicated in inattention, impulsivity,
and affective dysregulation.
Executive neurocognition can be divided into several subtypes (see Nigg, 2000; Posner &
Rothbart, 2000; Rothbart, Ahadi, & Evans, 2000). Nigg (2000) has proposed a useful taxonomy of
the major types of executive neurocognition. (A) Interference control involves the conscious,
deliberative control of one’s attention and motoric behaviors. The neural system that subserves this
function is the connection between the dorsolateral and orbitofrontal cortices and subcortical
structures, such as the anterior cingulate. The most well-known neurocognitive test of this function
is the Stroop Task (Stroop, 1935). In the Stroop task it takes an individual longer to name the ink
color of a color word printed in a differing color (e.g., naming the color blue when the word bredQ
is printed in blue ink) than a neutral stimulus (e.g., bxxxxQ) printed in the same ink color.1 (B)
Cognitive inhibition is the ability to suppress information from working memory. There are both
effortful and implicit types of this capacity. The effortful type is illustrated in the bdirected forgettingQ
task. This paradigm presents subjects with a series of words. After each word is presented, subjects
are instructed to either forget (F) or remember (R) the word, and then subjects are asked to recall as
many of the words that they can, regardless of what they were instructed to do initially. The implicit
version of cognitive inhibition is exemplified in the bnegative primingQ tasks (Tipper, 1985). For this
task, first, a person must respond to a stimulus (e.g., name the blue object and ignore the yellow
object). In the subsequent bprobeQ trial, the stimulus to be named is the same as the one that was
ignored in the previous trial. For instance, if the person suppressed a (blue) chair to name a (yellow)
car, they now are asked to name a (blue) chair. It takes more time for individuals to identify an
object after they have been asked to ignore it in a prior trial than when it was not presented in an
earlier trial. (C) Behavioral inhibition involves the inhibition of a cognitive expectation and/or
motoric behavior in order to follow a different behavioral directive, expectation, or cognitive rule.
Behavioral inhibition involves, but is not limited to, premotor areas their reciprocal connection to
lateral and orbitofrontal areas of the prefrontal cortex. An example of behavioral inhibition is the Go–
No-Go Task (Casey et al., 1997). This task requires a subject to bgoQ (e.g., press a button) when a
frequent stimulus (e.g., the letter bXQ) appears but to withhold a button response (bno-goQ) when an
infrequent stimulus (e.g., the letter bYQ) appears.
Motivational-affective inhibition is defined as the deliberative interruption of a propensity or
behavior due to a motivational–emotional state. A laboratory paradigm for affective inhibition is the
Emotional Stroop Test. In this version of a traditional Stroop task, reaction times are longer for
naming the ink color of emotion-related words or other psychopathologically relevant content
(Williams, Mathews, & MacLeod, 1996). An example of motivational inhibition is the Passive
Avoidance Task (Newman & Kosson, 1986), in which participants are instructed to use trial-and-error
to learn if responding to stimuli will result in monetary reward or loss. Passive avoidance errors refer
to the number of times that a participant responds to losing stimuli (commission errors). Misses refer
to the number of times that a participant failed to respond to a rewarding, or, winning stimuli
(omission errors).
2. Historical phases of cognitive inhibition and memory research on BPD
In the next section, we review and summarize the findings from three historical phases of research of
cognitive inhibition and memory in the borderline personality.
1
Due to space limitations we cannot summarize in detail the instructions and psychometric properties of all the referenced neurocognitive
measures. An excellent resource for this information is Spreen & Strauss (1998).
350
Table 1
Phase II studies of executive neurocognition and memory in BPD compared to control groups
Burgess (1990) Burgess (1991) O’Leary et al. (1991) Swirsky-Sacchetti et al. Carpenter et al. (1993)
(1993)
Gender (% female) 33% Not reported 81% 100% 100%
Diagnosis DSM-III-R DSM-III-R DSM-III-R DSM-III-R DSM-III-R
Interview Unstructured interview 2 independent evaluations, SCID II + DIB-R SCID II + DIB-R N6 Interview
unstructured N6 + impulsive
aggressive behavior
E.A. Fertuck et al. / Clinical Psychology Review 26 (2006) 346–375

Co-occurring Axis I No BPD group no concurrent - Substance - bacuteQ Axis I Yes, not specified
conditions excluded Axis I dependence in 2 years including MDD
- Current Affective d/o - Substance
dependence in 2 years
Medical/Neurological/ Not reported Not reported Cardiovascular, renal, HIV, neurological/medical N/A
Head trauma excluded hepatic, or seizure d/o known to affect cog-
disorder nition, head trauma, brain
injury
Matched normal Yes No (compared BPD to ma- Yes Yes N/A

control jor depression and schizo-
phrenia)
Group age differences Not reported Not reported No No Not reported
Psychiatric control No Yes Schizophrenia, No No No
and MDD
Medication status Off N1 week Not reported Off N2 weeks 8 subjects on meds Med free; unknown
length
Medication class Not reported Not reported Not reported 2 on 2 classes; 2 on 3 Not reported
classes
Setting Outpatient acute Outpatient acute Outpatient nonacute Outpatient nonacute Inpatient nonacute
Sample size 18 BPD, 14 Control 27 BPD, 20 16 BPD, 16 Control 10 BPD, 10 Control 17 BPD, 17 Control
Schizophrenia, 17 MDD
Control for Depression/ No No Co-occurring MDD Not reported
Affect/Other (N = 7) did not affect
results
Working Memory Yes No Yes Yes Yes

- Serial 7s; - 3 Step Commands - WAIS Digit Symbol - WMS-R Visual - WMS-R Visual
- Digit Span Memory Reproduction
No
- Immediate Repetition - WMS-R Associate

Learning
Delayed Memory Yes Yes Yes Yes Yes
- Delayed Memory - Delayed Memory; - Rey-Osterrieth - Rey-Osterrieth - Rey-Osterrieth
Screen
- (Embedded Figures) No No
- (Corsi Blocks) - WMS-R

- WMS-R Logical Logical Memory

Memory
Psycho-motor Skill Yes No Yes Yes Not Assessed
- Rhythm - Rhythm Reproduction - (WAIS Digit Symbol) - Luria Motor Skills
reproduction test
- Luria Motor No - Finger Tapping Test
Behavioral Inhibition / Yes Yes Yes Yes

Inhibitory Control/ - Perseverative - Omission Errors subtests - WAIS Picture - Trails A and B
Cognitive Inhibition Screening Test Arrangement
No No No No
- Similarities - WCST - WCST - WCST
- Serial 7 - Trails A and B - (CPT)
- Proverb Interpretation
Interference Control Not assessed Not Assessed Yes Yes No
- Embedded Figures - Stroop - CPT
Test
- Road Map
- Corsi Blocks
Affective Inhibition Not assessed Not Assessed Not Assessed Not Assessed Not Assessed
IQ Not assessed Not assessed Yes Yes Yes

- WAIS Performance - WAIS Verbal, - On three WAIS subtests
IQ Performance, and administered Digit Symbol,
Full Scale IQ Block Design lower in
BPD, but not Vocabulary
351
(continued on next page)
352
Table 1 (continued)
Judd and Ruff Van Reekum et al. Cornelius et al. Driessen et al. Sprock et al. (2000) Sprock et al. (2000)
(1993) (1996) (1989) (2000) Part I Part II
Gender (% female) 80% N/A 66% 100% 100% 100%
Diagnosis DSM-III Not reported DIB DSM-IV DSM-III-R DSM-III-R
Interview Interview + DIBN6 DIB N6 DIB N6 SCID-II SCID-II SCID-II

Co-occurring Axis I - Affective disorder, - Primary substance Substance Anorexia, Substance abuse, Substance abuse,
conditions excluded substance abuse, abuse, Peabody dependence, schizophrenina, psychotic disorder; psychotic disorder;
psychotic disorder Picture Vocabulary psychotic d/o, and schizoaffective, MDD Depressed group no Depressed group no
b80 bipolar d/o w/psychotic Sxs, other axis I or II d/os other axis I or II d/os
Medical/Neurological/ History of - Organicity, physical Seizure d/o, bphysical Infectious disease, Neurological, sensory, Neurological, sensory,
Head trauma excluded neurological d/o or disorders of known disorder with know endocrine d/o and motor d/os and motor d/os
head trauma excluded psychiatric psychaitric neurological d/o,
significance consequenceQ, mental head trauma, mental
retardation retardation
Matched normal Yes (archival control No No (test norms) Yes Yes Yes
control matched on gender,
age, and education)
Group age differences No Not reported No No Yes, BPD group older No
Psychiatric control No Yes No No Yes, current MDD or Yes current MDD or
Dysthymia Dysthymia
Medication status Off N2 weeks Not reported Off N1 week Off N1 week Not reported Not reported
Medication class Not reported Not reported Not reported Not reported Not reported Not reported
Setting Outpatient nonacute Inpatient nonacute Inpatient acute 18 inpatients, 3 Outpatient Outpatient
outpatients
Sample size 25 BPD, 25 Control 24 BPD, 11 TBI 24 BPD 21 BPD, 21 Control 18 BPD, 17 18 BPD, 18
Depressed, 16 Control Depressed, 18 Control
Control for Depression/ No Not reported No Yes Controlled for Age Controlled for
Affect/Other and WAIS Block education
Design and estimated IQ
Working Memory No No No No No No
- Controlled Oral - Digit Span - WAIS Digit Span - WAIS Digit Symbol - Rey-Osterreith Copy - Rey-Osterreith Copy
Word Association Test
- R Digit Span - WMS-Digit Span - WMS Visual Memory, - Story Recall Immediate
Associate Learning - WMS-Digital Span
- WAIS-R Digit Symbol
Delayed Memory Yes Yes No No No No
- Rey-Osterrieth - Rey-Osterrieth - Crosses - Rey Osterreith - Rey-Osterreith - Story Recall
- Star Drawing - WMS Logical —Delayed on Neutral
Memory Words
- Luria Selective (Total score for copy, - WMS Logical
Reminding Test immediate, and 5-min. Memory
- WMS-R Logical recall)
Memory

Psycho-motor Skill Yes Not assessed No No No Not Assessed
- (WAIS-R Block - Grooved Pegboard - (Digit Symbol Test) - Porteus Mazes
Design)
No - Finger Tapping Test
- Grooved Pegboard
- Finger Tapping Test
Behavioral Inhibition / Yes Yes Not Assessed No No Not Assessed
Inhibitory Control - Ruff figural fluency - Trails A and B (time - (Block Design) - Porteus Mazes
Cognitive Inhibition to complete)
No No - Trailmaking B
- Trails A and B
(errors)
- WCST (number of
correct sorts)
Interface Control No Not assessed Not Assessed No Yes Not Assessed
- Stroop - Embedded Figures - Stroop (Neutral
Words), (Depressed
also impaired on
this task)
Affective Inhibition Not Assessed Not assessed Not Assessed Not Assessed No No
- Emotional Stroop - Word Recall
emotional vs. neutral
- Story Recall:
positive, negative,
and neutral; immediate
and delayed
IQ No Not assessed Not Assessed No Yes No
WAIS-R - WAIS-R - WAIS-R Vocabulary - WAIS-R Vocabulary
Information, Similarities, and Block Design; BPD and Block Design
Picture completion, and better than Depressed
Block Design subtests Group on Block Design
353
2.1. Phase I: phenomenological description of the BPD construct
We have characterized Phase I, before the DSM-III definition of BPD, as one of the phenomenological
descriptions. The broad class of bborderlandQ disturbances began to be described in the late 19th Century
(Stone, 1986). Later, Kernberg (1967, 1976, 1996), based on the approaches of descriptive psychiatry
and psychoanalytic theory, proposed a pioneering and still influential definition of borderline personality
organization (BPO), a forerunner of the current BPD nomenclature. During Phase I, standard
psychological testing assessed cognition and perception in BPO, most often utilizing the Wechsler Adult
Intelligence Scales (WAIS; Wechsler, 1955) and the Rorschach Inkbot Test. Using these measures,
borderline subjects were reported to exhibit relatively intact intellectual performance on the WAIS, but
disturbed or deviant Rorschach responses (Rapaport, Gill, & Schafer, 1968). Subsequent reviews of this
early Rorschach research (Gartner, Hurt, & Gartner, 1989; Widiger, 1982) have questioned whether the
subjects in these studies would be considered BPD by DSM standards, and the methodology and data
analysis.
Gunderson and Singer (1975) reviewed the literature on the diagnostic indicators of BPD, and this
effort ultimately led to the DSM-III (American Psychiatric Association, 1980) criteria for BPD. This
review brought an organizational focus to previously disparate observations of BPD, and helped inspire
an interest in a more behavioral and reliable approach for classifying borderline personality, and
increased the reliability of the BPD diagnosis. Phase I of research in BPD concluded with the emergence
of a consensus that a BPD was a disorder that had some syndromal qualities worthy of further clinical
attention, both in terms of description and assessment. However, assessment methodologies for the
diagnosis of BPD were in their infancy and there was no laboratory science of BPD.
2.2. Phase II: studies that utilized comprehensive neuropsychological batteries to compare BPD to other
psychiatric and control groups
With the advent of the DSM-III (American Psychiatric Association, 1980) and the Axis II system with
its explicit batheoreticalQ criteria, a categorical approach that often used behavioral criteria was initiated
in the psychiatric classification of the disorder. This period corresponded to a shift in psychiatry to an
empirical research perspective that emphasized reliability, validity, and psychometric efficiency
(Cronbach & Meehl, 1955; Meehl & Rosen, 1955). As a result of this focus there was increased
standardization and reliability of psychiatric diagnosis by semi-structured interviews (e.g., IPDE;
International Personality Disorder Examination; Loranger, 1999) and self-report instruments (e.g.,
Millon Clinical Multiaxial Inventory-III; Millon, Davis, & Millon, 1997). Concurrently, during the
1980s, the neuropsychological test batteries evolved to assess a wide range of functions in a more
principled manner and were increasingly applied to psychiatric populations.
Ten publications and conference presentations were identified from this phase of research. Criteria for
inclusion here included an assessment of BPD as defined by either the DSM or the International
Classification of Diseases (ICD) diagnostic systems, comparison with a non-clinical control group and/
or a psychiatric comparison group, and publication or presentation in a peer-reviewed scientific
publication or meeting. PsycINFO and Medline databases and references from previous review chapters
were used to identify studies. Table 1 summarizes the 10 (with one study, Sprock, Rader, Kendall, &
Yoder, 2000, reporting two studies in the same paper) peer-reviewed publications and conference
presentations from Phase II.
2.2.1. Methodological comparison between significant difference (SD) and no significant difference
(NSD) studies in phase II
There were several studies in Phase II which documented inhibitory and/or memory deficits the
BPD group relative to control groups (Burgess, 1990, 1991; Carpenter, Gold, & Fenton, 1993; Judd &
Ruff, 1993; O’Leary, Brouwers, Gardner, & Cowdry, 1991; Swirsky-Sacchetti et al., 1993; Van
Reekum et al., 1996) which we label the Significant Difference (SD) studies. There were also several
studies that did not find statistically significant deficits in BPD groups compared to control groups
(Cornelius et al., 1989; Driessen et al., 2000) which we label Non-Significant Difference Studies
(NSD). Overall, the SD and NSD studies used comparable methodologies with reasonably well
characterized patient groups. However, the NSD studies appear to have more carefully addressed
confounding factors such as neurological and medical history, Axis I co-occurrence, and IQ
differences. Additionally, the NSD studies appear to have utilized a higher percentage of female
participants compared to the significant studies. These observations suggests that predominantly
female BPD samples with fewer co-occurring conditions are less likely to demonstrate neurocognitive
impairments relative to comparison groups. However, in clinical settings BPD cases without co-
occurring conditions are rare, raising question about the representativeness of these BPD samples.
Additionally, three of the four studies in the SD group that assessed IQ found relative deficits in the
BPD group when compared to the control group. By contrast, only one of three studies that assessed
IQ in the NSD group exhibited this problem, and, in this study, IQ was used as a covariate in an
attempt to control for its effect on neurocognitive performance (Sprock et al., 2001, Study I). We,
consequently, speculate that group IQ differences may account for some of the apparent findings
comparing the BPD and control groups in the significant group of studies.
Recognizing the limitation of focusing primarily on null hypothesis significance testing (Rosenthal,
Rosnow, & Rubin, 2000), we also evaluated the effect sizes of the Phase II studies. Five of the ten
studies reported means and standard deviations for both a BPD and comparison group. Based on these
data, Table 2 summarizes effect sizes (Cohen’s d; Rosenthal et al., 2000) that were calculated on
executive neurocognition and memory domains, contrasting the BPD with the comparison groups
(clinical or normal control). We conducted a preliminary meta-analysis of Cohen’s d effect sizes within
each memory and cognitive domains. For each study, a mean domain effect size was calculated (some
studies had several instruments in one domain, others had none). These study domain means were then
averaged, yielding a mean domain effect size across all studies (see the last row of Table 2). These
preliminary mean effect sizes indicate that BPD groups perform more poorly across executive
neurocognition and memory domains compared to contrast groups. The largest effect size is in the area
of delayed nonverbal memory, which is in the blargeQ range by conventional effect size standards. Other
domain effect sizes are at least in the bmediumQ range. This preliminary meta-analysis indicates that
memory and cognitive inhibitory weaknesses are commonly detected in BPD, but a distinct
configuration of deficits does not emerge.
In summary, while memory and executive neurocognitive impairments appear common in at least
subgroups of BPD subjects, the inconsistent findings from Phase II do not clearly implicate any particular
executive neurocognitive or memory system impairment in BPD. Further caution is warranted considering
that individuals with other clinical syndromes can exhibit comparable impairments in executive
neurocognition and memory functions—including subtypes of geriatric depression (e.g., Kiosses,
Klimstra, Murphy, & Alexopoulos, 2001) and schizophrenia spectrum disorders (e.g., Lenzenweger,
Cornblatt, & Putnick, 1991; Park, Holzman, & Lenzenweger, 1995; Trestman et al., 1995).
356
Table 2
Effects size (ES; Cohen’s d) of BPD compared to control groups in executive neurocognition and memory systems in phase II studies
Study; Sample Working Memory- ES Working Memory- ES Delayed Memory- ES Delayed Memory- ES Behavioral-Cognitive ES Interference ES
Verbal Non-verbal Verbal Non-verbal Inhibition Control
Burgess, 1991; Digit Span 0.58 Rhythm 0.46 Delayed Memory 1.44 Perseveration errors 0.57 Serial Sevens 0.58
27 BPD; 20 MDD Immediate Repetition - 1.25 Reproduction Irrelevant addition - 0.35 subtraction

errors
Three-Step Commands 0.14 Omission errors 0.88
Inversion errors 0.68
O’Leary et al., 1991; Digit Span 0.09 Digit Symbol 1.27 WMS 1.45 Rey O 0.98 WCST 0.92 Embedded Figures 1.06
16 BPD; 16 Control WMS 0.77 Seashore Test 0.24 - Delayed Logical - Delayed Recall - Categ. achieved 0.29 - Score 0.93
- Logical Memory 0.43 - Rhythm 0.55 Memory - Persev. Errors 0.55 - No. of failures
- Digits Forward 0.63 - Tonal memory 1.12 - Nonpers. Errors 0.45
- Digits Backward Rey O. - Trials to first cat. 0.30
- Recall - Unique responses 0.06
- Failure to maintain
set
Swirsky-Sacchetti WMS 2.0 WMS 1.14 WMS 0.10 WMS 0.88 Trails B 0.37 Stroop Color-Word 0.52
et al. (1993); - Logical Memory - Figural Memory 0.37 - Delayed Logical - Delayed Figural WCST 0.00 - Word 0.54
10 BPD; 10 Control Rey Memory Memory - No. categories 0.53 - Color 0.71
- Recall - No. Errors - Color-Word 0.37
Verbal Learning - 0.12
- Emotional Interference
- Neutral Interference
Judd and Ruff (1993); Selective reminding 0.65 Rey O. 1.07a Selective reminding 0.13 Stroop Test 0.15
25 BPD; 25 Control test test
- Sum recall 0.14 - Immediate Recall 0.09 - Delayed recall - Time 0.32
Digits Span Seashore Rhythm 0.93 - Error
Digit Symbol 1.19
Ruff Figural Fluency
Driessen et al., 2000; WMS Immediate 0.95 Digit Symbol 0.87 Rey O. 0.28 WMS Delay 0.80 Embedded Figures
21 BPD; 21 Control Rey-Immediate 0.27 - Delayed - Time/figure 1.02
Recall - No. Errors 0.83
- No. Repeats 0.58
Cohen’s d Domain 0.73 0.68 0.68 0.89 0.39 0.61
Mean for all Studies
Cohen’s d utilized for effect size calculation, using a pooled standard deviation from BPD and comparison groups.
a
There was a probable error in the decimal place of the standard deviation reported in this study. The effect size here is based on a presumed correction, but should be considered speculative.
2.3. Phase III: recent studies of executive neurocognition and memory systems in BPD
During the period from 1999 to the present, studies investigated executive neurocognition and
memory systems to BPD in a more differentiated and ecologically valid manner than the Phase II studies.
Another characteristic of Phase III is a move away from conventional neuropsychological assessment.
This is most apparent in the use of instruments that assess the influence of motivation, emotional state,
affective valence, and episodic memories in BPD and comparison groups.2
2.4. Executive neurocognition
2.4.1. Cognitive interference control

Posner et al. (2002) report that BPD subjects (without current mood disorder; n = 39), compared to
healthy control participants (n = 30), are specifically deficient in a neural network associated with the
voluntary inhibition of thoughts and behaviors. These researchers utilized the Attention Network Task
(ANT; Fan, McCandliss, Sommer, Raz, & Posner, 2002) laboratory test, which assesses three
independent attentional functions. The first is alerting, the capacity to sustain an alert cognitive state.
The second is orienting, which involves focused identification and selection of sensory stimuli. The third
is conflict which is the capacity to voluntarily decide among competing responses based upon a principle
or goal, using a visual flanker task. The anterior cingulate is a brain region which is essential to cognitive
interference controls as measured by a conflict task (Botwinick, Braver, Barch, Carter, & Cohen, 2001)
such as in the ANT. The BPD participants in the Posner et al. (2002) study were specifically impaired
relative to control participants in the conflict task as assessed by the ANT. Further, a group of individuals
who exhibited temperamental features similar to BPD (n = 22), yet did not meet criteria for BPD,
performed better than the BPD group on the conflict index of the ANT. However, the temperamentally
matched group was not significantly different from the other two groups on this conflict task.
2.4.2. Cognitive inhibition/encoding

There have been three studies of cognitive inhibition and encoding in BPD. Cloitre, Cancienne,
Brodsky, Dulit, and Perry (1996) studied a DSM-III-R diagnosed BPD sample of 48, comparing those
who had and had not reported experience of childhood sexual abuse (24 each), to a healthy control group
of 24 subjects. The study utilized the experimental bdirected forgetting paradigm,Q which has been
described previously. In this study, words were presented with positive, neutral, and negative emotional
valences. The BPD group with a history of abuse had better recall of neutral words they were asked to
remember relative to the non-abused BPD group and the control group. Additionally, across the total
sample, the number of Remember-Neutral words recalled was positively correlated with self-reported
dissociative experiences. The authors argue that, among traumatized BPD subjects, the ability to shift
attention from distressing memories of abuse to more neutral, dissociated sensory experiences allows for
the maintenance of positive memories of caretakers and the avoidance/suppression of negative memories.
While this is one plausible interpretation of the findings, it would be strengthened if the traumatized BPD
group also had remembered fewer negative words they were asked to remember. Further, since the finding
2
Two recent studies of executive neurocognition in BPD are not reviewed here due to the methodological drawbacks of lack of semi-
structured diagnostic assessment of BPD (Dinn et al., 2004) and the use of unconventional cut off scores to make the BPD diagnosis (Kunert,
Druecke, Sass, & Herpertz, 2003, see p. 500).
was only apparent in the traumatized BPD sample, it is unclear if this is a marker of BPD or of a history of
childhood trauma independent of diagnostic status.
Korfine and Hooley (2000) compared 22 day hospital and 23 community ascertained DSM-IV BPD
subjects (diagnosis was established using the IPDE; Loranger, 1999) to 20 healthy control subjects, also
utilizing the directed forgetting paradigm. This directed forgetting procedure utilized valenced words
that were positive, borderline salient (e.g., abandon, reject, and cruel), negative, and neutral. The BPD
subjects were found to be more likely to remember borderline salient words they were told to forget than
normal subjects. These findings suggested enhanced encoding of BPD salient stimuli and, perhaps, a
disinhibition in forgetting borderline salient words. This is the first study to show an affective cognitive
inhibition bias in BPD. The findings from this study are consistent with the Emotional Stroop findings in
BPD (Arntz, Appels, & Sieswerda, 2000) summarized below.
2.4.3. Behavioral inhibition

Consistent with these findings, BPD subjects (without current mood disorder; n = 24) exhibit relative
deficits in cognitive planning and set-shifting functions on the Wisconsin Card Sort Test (WCST;
Heaton, 1981) compared to healthy control subjects (n = 68; Lenzenweger, Clarkin, Fertuck, &
Kernberg, 2004). These BPD subjects evidenced no significant differences with control participants on
other measures of spatial working memory and sustained attention. This study also found that BPD
individuals exhibit significantly higher levels of negative affect, lower levels of positive affect, and
lower levels of non-affective constraint (an index of behavioral inhibition) as assessed by the self-report
Multidimensional Personality Questionnaire (MPQ; Tellegen, 1982) as compared to population norms.
Additionally, non-affective constraint on the MPQ was negatively associated with performance on the
WCST indexes in this BPD sample.
Two reports (Lenzenweger et al., 2004; Posner et al., 2002) drew from the same BPD patient pool.
Twenty-two BPD subjects from this pool completed both the ANT and WCST protocols. In this BPD
sample, the number of BPD criteria met was associated with more impaired attentional performance on
the ANT (Fertuck, Lenzenweger, & Clarkin, 2005). These associations were independent of the effects
of age and medication status (approximately half the BPD subjects in these studies were on medication).
2.4.4. Motivational cognitive inhibition

Four studies have investigated motivational cognitive inhibition in BPD utilizing an experimental
design. In the first study, (Dougherty, Bjork, Huckabee, Moeller, & Swann, 1999), 14 hospitalized
female BPD subjects were compared to age, race, and education level matched control participants on
several aggression and impulsivity measures. One lab task utilized was the Impulsivity Task (IT; Cherek
& Dougherty, 1997) which offers participants a choice between immediate vs. delayed monetary
rewards, where the delayed rewards are larger. During the task, the larger reward is progressively
delayed. On the IT task, the BPD subjects responded to avoid longer delays for reward than the controls,
but were otherwise similar to the controls.
Using another laboratory paradigm, the passive avoidance task (described previously), Hochhausen,
Lorenz, and Newman (2002) compared incarcerated females with (n = 39) and without BPD (n = 127) on
this passive avoidance task. They found that the BPD group exhibited significantly more errors in
responding to the non-winning numbers that the controls. Further, there was a trend towards the BPD
group also failing to respond to winning numbers. Accordingly, the BPD group also reported more
impulsive behaviors. The errors in responding to non-winning numbers in this BPD sample are similar to
deficits identified in psychopathy on the passive avoidance task. However, the fact that BPD individuals
also exhibited fewer responses to reward (errors of omission) in this study is not typically found with in
psychopathic groups. The authors conclude that BPD subjects may be impulsive predominantly in their
disinhibition in avoiding punishments. This finding may explain why the Dougherty et al. (1999) study
did not find that the IT task was related to impulsivity in BPD. The IT task does not assess the inhibition
of responding to non-reinforced (as opposed to reinforcing) stimuli.
In the context of a serotonin synthesis study in BPD, participants were assessed using a computerized
go/no-go task of behavioral inhibition (Leyton et al., 2001). Eleven healthy control participants (6
women and 5 men) were compared to 13 medication-free BPD subjects (8 women and 5 men). The BPD
group was not currently depressed. The go/no-go task requires one to learn, based on rewards and
punishment, when to respond and not to respond to a stimulus. Punishment–reward commission errors
represent an error in inhibiting a response that will be punished, based on prior learning. The BPD group
committed significantly more punishment–reward commission errors than the control group. Serotonin
synthesis was associated with these same go/no-go errors, specifically in the medial frontal gyrus,
anterior cingulate gyrus, temporal gyrus, and striatum.
Executive and motivational cognitive inhibitions were compared in 42 BPD (without current
depression) and 42 healthy control participants (Bazanis et al., 2002). Motivational inhibition was
assessed with a decision making task which asked participants to make bbetsQ on choosing whether a
token is hidden in one of two boxes. In the ascending phase of the task bets become progressively larger.
A descending phase involves the bets becoming progressively smaller. The instrument assesses
deliberation time, the proportion of responses on which the participant bet the most likely outcome, the
amount the participant bet, and the extent to which participants bet risky vs. less risky amounts of money.
Participants in this study were also administered a Tower of London planning task, and a visual
recognition memory task. The BPD subjects took significantly longer to decide upon the bets, they chose
the most likely outcome significantly less often than the control group participants, and they responded
more often to the early bets than the later. The BPD subjects also did more poorly on the Tower of London
task than the control subjects. There were no differences in visual recognition memory between the two
groups. These results are consistent with the three prior studies of motivational cognitive inhibition in
BPD, and the Tower of London findings reinforce non-motivational deficits in behavioral inhibition.
2.4.5. Affective-cognitive inhibition

Finally, using the Emotional Stroop Test paradigm, Arntz et al. (2000) tested the hypothesis that 15
BPD individuals would exhibit more difficulty in processing negative emotion words than neutral words
compared to 15 healthy controls and to 12 participants with Cluster C personality disorders. They used
four classes of negative words, three of which were BPD salient: negative views of others, negative
views of self, sexual abuse-related words, and general negative words. Words were presented both
supraliminally (at an interval that can be registered in consciousness) and subliminally (at an interval
shorter than can be consciously registered). They found that both the personality disordered groups
exhibited significantly more difficulty processing the supraliminally, but not subliminally, presented
emotion words. The study suggests that emotional valence impairs the interference control subtype of
executive neurocognitive processing in BPD and Cluster C personality disorder individuals compared to
controls. The study did not find differences between the personality disordered groups on this task,
which may indicate either a lack of statistical power, or that performance on this version of the
Emotional Stroop is associated with personality disorder more broadly defined.
2.5. Memory systems
Experimental investigations of memory systems and BPD are few in number. The studies that have
been conducted have focused on autobiographical–episodic and semantic memory and encoding in BPD
subjects.
2.5.1. Autobiographical–episodic memory

Heard, Startup, Swales, Williams, and Jones (1999) compared 23 BPD subjects to 23 matched
controls (18 females and 5 males were in each group) on episodic–autobiographical memory. To
measure autobiographical memory the investigators utilized the Autobiographical Memory Test (AMT;
Williams & Broadbent, 1986). In the AMT, subjects are asked to recall episodic–autobiographical events
related to the cue words. A bspecificQ memory happened on a particular day, and a bgeneralQ memory
happened repeatedly or over extended periods of time. These investigators predicted that BPD
individuals with dissociative symptoms would exhibit less retrieval of specific autobiographical
memories, or, conversely, more general autobiographical memories. The BPD group demonstrated
significantly more bgeneralQ episodic–autobiographical memories on the AMT and also exhibited higher
levels of trait anger, depression, and anxiety, and dissociative experiences than the control group. In
addition, bgeneralQ memories were correlated with dissociative experiences. In assessing cue valence,
BPD subjects produced more general memories to negative cues than the control group. This pattern of
findings is consistent with responses by subjects with PTSD and Acute Stress Disorder (ASD; e.g.,
McNally, Lasko, Macklin, & Pitman, 1995). A weakness of the study is that there was no assessment of
history of traumatic experiences.
In a follow-up study, Startup, Heard, Swales, and Jones (2001) assessed BPD subjects with a history
of parasuicide (18 females and 5 males) using the Autobiographical Memory Test (AMT; see above).
Contrary to their hypotheses, these investigators found that bspecificQ recall of episodic memories, higher
levels of anxiety and depression (but not anger), each independently contributed to the prediction of
increased number of suicide and parasuicidal behaviors. If self-injury is triggered by specific, concrete,
and detailed recall of negative, traumatic episodes, these authors argue that more bgeneralQ recall of
memories may be part of an affect regulatory strategy that prevents self-injury.
While the above studies suggest that BPD individuals produce over-general autobiographical
memories with negative memory cues, another study suggests that BPD participants do not exhibit over-
general autobiographical memories using only neutral cue words (Arntz, Meeren, & Wessel, 2002). This
pattern of findings further reinforces the importance of considering affective valence in the memory
processing of BPD, as negatively valenced memories appear to have a more influential effect on the
form of autobiographical memories than neutral memories. Similar to the Cloitre et al. (1996) study, the
autobiographical memory studies suggest a link between BPD and the impaired encoding and retrieval
of negatively valenced episodic memories, possibly leading to the clinical manifestation of dissociation.
These studies also establish the utility of an experimental approach using laboratory memory tasks as
indicators of risk factors and to investigate patterns of memory consolidation and dissociation in clinical
and non-clinical subjects.
2.5.2. Memory and neurocognitive deficits in bpd with current major depression
Whether co-occurring major depression (MDD) exists is crucial in investigating memory and
neurocognition in BPD, as MDD is the most common co-occurring disorder in BPD (cf.
Zimmermann & Mattia, 1999). MDD is characterized by deficits in episodic and semantic
(declarative) memory, verbal fluency, and attentional performance relative to healthy control groups
(see Zakzanis, Leach, & Kaplan, 1998 for review). Two studies have focused on comparing current
MDD to current MDD with co-occurring BPD on memory and neurocognitive domains. In the first
study, memory functions with positive, negative, ambivalent, and neutral words were compared in
three groups: 40 subjects with symptoms of major depressive disorder (MDD; 20 subjects with a
comorbid diagnosis of BPD and 20 subjects without BPD), and 20 control participants (Kurtz &
Morey, 1999). The two patient groups exhibited comparable severity of depressed mood, general
level of distress, and co-occurring psychiatric conditions. Forty-eight words (12 in each valence
category) were presented to the participants on a computer. This was followed by a free recall 5 min
after the presentation, and a recognition recall (including 48 distracter words) 50 min after the
presentation. The investigators identified more impairment in recall and recognition memory among
the BPD with MDD group compared to the control group. There was also greater impairment in
recognition memory in the MDD with BPD group compared to MDD subjects without BPD.
Controls and BPD subjects showed a positive word selectivity in recall, while MDD subjects showed
nonsignificant selectivity differences.
In the second study (Fertuck et al., 2005, submitted for publication), 55 subjects with MDD (33 of
these subjects did not meet criteria for any DSM-IV Axis II Personality Disorder [PD], and 22 met
criteria for BPD) were administered a comprehensive neuropsychological battery that assessed 7
domains of performance: attention, working memory, general intellectual functioning, memory,
executive cognitive control, psychomotor skill, and motor skill. Additionally, the mood state was
assessed. MDD with BPD subjects reported higher levels of state anger, anxiety–tension, and higher
levels of overall negative affect than individuals with MDD without PD. While neuropsychological
performance appeared similar in these two groups in standard group comparisons, when levels of anxiety
were controlled, BPD-MDD subjects exhibited superior general intellectual performance, psychomotor
speed, and attention. The impact of anxiety on neuropsychological performance in BPD further
reinforces the need for future experimental studies of the effects of mood on cognitive function in BPD.
Such research is required to determine whether mood dysregulation, rather than core depressive
symptoms, underlies cognition impairments in BPD.
2.6. Integrative summary of the three phases
During Phase I the phenomenology of BPD was described and the stage was set for more systematic
studies of executive neurocognition, memory, and BPD. Phase II compared well-characterized BPD
groups to controls on comprehensively assessed, non-affective neuropsychological performance.
Compared to controls, BPD subjects studied in this Phase did not demonstrate a consistent constellation
of deficits in executive neurocognition or memory. A preliminary meta-analysis suggests that BPD
groups are more compromised than controls in all measured executive neurocognition and memory
domains, with effect sizes in the medium to large range. A lack of specificity and sensitivity of findings
from the Phase II research highlights the importance of studying the impact of affective stimuli and
arousal, risk factors, and co-occurring conditions associated with BPD, which has begun in the current
Phase III. While the Phase III studies provide interesting leads and results regarding the impact of affect
on cognition and memory in BPD, none of the studies have been replicated, and should be considered
preliminary.
Summary of Phase III findings:
1. Preliminary reports consistently point to impaired executive neurocognition in BPD, independent of

affective influences (Bazanis et al., 2002; Lenzenweger et al., 2004; Posner et al., 2002). In these
studies of non-depressed BPD subjects, other basic cognitive processes (working memory, attention,
etc.) remain relatively intact under affectively neutral conditions. Further, the extent of BPD
pathology appears associated with greater impairment in attentional and cognitive interference control
performance (Fertuck et al., 2005).
2. There is enhanced encoding and impaired cognitive inhibition of negatively valenced emotional
stimuli in BPD relative to healthy control subjects (Korfine & Hooley, 2000).
3. Motivational (Bazanis et al., 2002; Dougherty et al., 1999; Hochhausen et al., 2002; Leyton et al.,
2001) and affective (Arntz et al., 2000) cognitive inhibition are compromised in BPD compared to
control participants. Moreover, poorer performance in motivational cognitive inhibitory performance
is associated with behavioral indices of impulsivity in BPD (Hochhausen et al., 2002).
4. Negatively valenced episodic memories in BPD appear less specific than in control participants
(Heard et al., 1999). Additionally, greater specificity in the recall of episodic memories contributes to
the prediction of increased number of suicide and parasuicidal behaviors in BPD (Startup et al., 2001).
5. BPD subjects in an episode of MDD appear similar in neurocognitive performance to uncomplicated
MDD, yet are also more affectively aroused than MDD. Elevated anxiety, when controlled for in
BPD, highlights that BPD subjects perform better than uncomplicated MDD in psychomotor,
attentional, and general intellectual performance (Fertuck et al., 2005, submitted for publication).
3. General discussion
Several questions emerge from the existing studies. (1) How does the literature on executive
neurocognition and memory contribute to the understanding of BPD from developmental and
neurobiological perspectives? (2) What are the implications of these findings for modeling BPD and
refining the taxonomy of BPD in relation to neighboring disorders? (3) What is the clinical relevance of
these findings? (4) Can clinical perspectives of BPD help guide future research in this area?
3.1. Neurobiological and neuroscience approaches
Current theories of BPD emphasize emotional dysregulation (cf., Linehan, 1993; Westen, 1994;
Westen, Muderrisoglu, Fowler, Shedler, & Koren, 1997) and are not as explicit about the potential for
mutually interacting impairments in executive neurocognition and memory disruption. Depue and
Lenzenweger (2001, 2005) have proposed that BPD and other personality disorders arise out of an
interaction between multiple neurobehavioral systems. They posit that BPD is an emergent phenotype
reflective of a highly reactive negative affectivity system, high levels of social fear, low levels of positive
affect, and low levels of non-affective constraint. This model emphasizes the interaction between these
processes as crucial to understanding the phenomenology of BPD. Central to the study of executive
neurocognition, a non-affective constraint system has been conceptualized from a neurobiological
perspective as the central nervous system’s primary modulator or regulator of motor behavior, positive
and negative affect systems, and cognition (Depue & Lenzenweger, 2001, 2005). The existence of a non-
affective constraint system is supported by research in both personality theory (e.g., Tellegen & Waller,
in press) and neurobiological theory (Depue & Lenzenweger, 2001, 2005), with an emphasis on the
influence of serotonin (Depue & Collins, 1999).
Another highly relevant circuit is stress responsiveness of the hypothalamic pituitary adrenal (HPA)
axis. Individuals with a long history of excessive social stress, such as would occur in childhood trauma,
are vulnerable to HPA hyperreactivity (Putnam & Trickett, 1997). With such hyperreactivity, there is an
overly rapid transition from inhibition and planning to reflexive, fight-or-flight action. The neural
mechanism related to this is related to a switch from prefrontal, inhibitory to posterior-limbic, affective
processing (Mayes, 2000). Executive neurocognitive capacities may be seriously compromised at
relatively low levels of emotional arousal in BPD, manifested in a premature shift to fight-or-flight
emotional states in response to threateningly perceived stimuli.
In partial support of this conceptualization, BPD individuals with a history of childhood trauma,
compared to both BPD individuals without a history of childhood trauma and healthy controls, have
demonstrated higher adrenocorticotrophic hormone (ACTH) and cortisol response to a combined
dexamethasone/corticotropin releasing hormone (DEX/CRH) test (Rinne et al., 2002). Chronic HPA
reactivity also influences episodic (particularly spatial) and semantic (often called declarative) memory
encoding, possibly due to dendritic cell atrophy in the hippocampus (McEwen, 1999). This would seem
in accord with our finding that, compared to controls, BPD participants exhibited the largest deficits in
delayed nonverbal memory performance, with an effect size in the large range. Compellingly, there is
corroborating evidence for hippocampal cell atrophy in BPD individuals who have been traumatized in
that three volumetric brain imaging studies have found smaller hippocampal volumes in BPD subjects
compared to control subjects (Driessen et al., 2000; Schmahl, Vermetten, Elzinga, & Bremner, 2003; van
Elst et al., 2003). These studies, however, do not address the question of whether reduced hippocampal
volume is in itself a pre-existing vulnerability (cf. Gilbertson et al., 2002) or, a consequence of adverse
experience. Another possibility is that such hippocampal atrophy is primarily due to chronic depressive
symptoms.
Finally, biological, neuroendocrine, and imaging studies provide evidence for the involvement of
serotonergic activity in impulsive aggression (Coccaro et al., 1989; Gurvits, Koenigsberg, & Siever,
2000; Siever & Trestman, 1993) in working memory, and inhibitory processes (Depue, 1995; Depue &
Lenzenweger, 2001, 2005). Consequently, compelling areas for research are in the interface of relevant
neurobehavioral systems, such as the serotonergic system, the HPA circuit, non-affective constraint,
negative affectivity, and impulsive-aggression in BPD and related disorders.
3.2. Neuroimaging
The functional neuroimaging of cognitive and memory processes can elucidate their neural substrates.
There are reports of high reactivity of the amygdala in processing social-affective stimuli in BPD using
functional magnetic resonance imaging (fMRI; Donegan et al., 2003). With respect to emotional
reactivity and impulsivity, a preliminary fMRI study of BPD subjects compared to healthy controls
suggests a disrupted interaction between the arousal of negative affect (the amygdala) and the affect
regulating capacities of inhibitory systems (dorsolateral and orbitofrontal cortex) using a emotionally
valenced variation of a go/no-go cognitive and task (Silbersweig et al., 2002). Amygdala reactivity to
emotional stimuli may discriminate BPD from antisocial individuals, who fail to show physiological
activation to sad faces and lack empathy for the distress of others (Blair, Jones, Clark, & Smith, 1997).
The instruments reviewed in the domains of executive neurocognition and memory systems in BPD can
provide challenge paradigms for imaging studies. Conversely, imaging findings may inform the types of
cognitive and memory processes to study in more differentiation, such as the spatial and
autobiographical encoding that is facilitated by the hippocampus.
3.3. Developmental influences on executive neurocognition and memory in BPD
3.3.1. Genetics
The development and acquisition of higher order cognitive functions such as working memory,
attentional systems, and aspects of cognitive inhibition appear to be powerfully influenced by genetics
(e.g., Goldsmith, Lemery, Buss, & Campos, 1999; Gottesman, 1997). Further, there is evidence of strong
familial association of impulsivity and affective instability in BPD (Silverman, Pinkham, Horvath, &
Coccaro, 1991). It is plausible that genetically influenced deficits in inhibitory processes may contribute
to heritable differences in impulsivity and affective instability in BPD and related disorders. Another
potential outcome of a focus on neurocognition and memory processing in BPD is the identification of
endophenotypes (Gottesman & Gould, 2003; Gottesman & Shields, 1972) for BPD that can inform
genetic and risk factor studies of the development of BPD. An endophenotype is a reliable and valid
marker of liability for a form of psychopathology that is not visible to the unaided, naked eye (i.e., it
requires instrumentation or an advanced technology for detection). This concept has long been
influential in research on schizophrenia and schizotypy (Lenzenweger, 1999; Lenzenweger et al., 1991)
and has recently been adopted by those with an interest in BPD (e.g., Siever, Torgersen, Gunderson,
Livesley, & Kendler, 2002).
3.3.2. Temperament
Posner, Rothbart, and colleagues (Posner & Rothbart, 2000; Rothbart et al., 2000), within a
framework of temperament theory, describe effortful control as involving any deliberative inhibition of a
dominant task to perform a subdominant task. The effortful control aspect of temperament complements
more established aspects such as emotional reactivity and sensitivity. Effortful control allows for restraint
in the face of immediate, emotionally arousing rewards or punishments to obtain a longer-term goal.
This approach shares many similarities to the model proposed by Depue and Lenzenweger (2001). While
there are similarities between effortful control and non-affective constraint, they are not synonymous.
Effortful control is a deliberative process whereas the constraint concept relates to a neurobiological
system that affects and is impacted by other systems.
The temperament perspective has yielded compelling findings with infants and young children that
have direct implications for understanding BPD as developing from transactional influences between
genes, temperament, biological maturation, and social experience. Kochanska (1997) has demonstrated
that children’s capacity to understand the emotional state of others and their capacity for prosocial
interactions arise out of temperaments involving high levels of effortful control. By contrast, a
temperament high in negative affective intensity and reactivity and low in voluntary control over
behavior would appear to pave the way for impaired social interactions with peers and adults.
Accordingly, this may also be a temperamental disposition paving the way for the expression of BPD
(Fertuck et al., 2005; Posner et al., 2002; Lenzenweger et al., 2004). However, additional genetic and
environmental factors are likely involved (Clarkin & Posner, 2005). In a retrospective study of 18-year-
old young adults, structural modeling of the developmental predictors of adult BPD found that the
temperamental dimensions of disinhibition (or, low effortful control) and increased levels of negative
affectivity operate in concert with childhood abuse, parental disinhibitory disorder, and parental mood
disorder to predict the expression of adult BPD (Trull, 2001).
3.3.3. Adverse early experience

The association between childhood adversity (trauma and neglect) and the adult BPD diagnosis is
strongly established, with up to 9 of 10 BPD subjects reporting having endured abuse or neglect
(Zanarini et al., 1997).3 There is now other evidence that impairments in executive function, when they
exist in the context of such traumatic and adverse childhood experience, further predispose children to
BPD features. Zelkowitz, Paris, Guzder, and Feldman (2001) demonstrated that deficits in executive
function (on a childhood version of the WCST) and the experience of psychological trauma or neglect
made significant and independent contributions to predicting an increased level of borderline pathology
in these children.
3.3.4. Attachment organization

The security of adult attachment organization is frequently disrupted in BPD (see Agrawal, Gunderson,
Holmes, & Lyons-Ruth, 2004 for review). In convergence with temperament researchers, contemporary
attachment researchers have proposed that the quality of early attachment organization can impact the
development of cognitive capacities such as effortful control (Fonagy, 2003). Further, they argue the
impact of trauma and disrupted attachment security initiates a developmental pathway leading to adult
BPD, particularly its interpersonal dimensions. Interestingly, a gene that is implicated in dopaminergic
processes, the DRD4, is associated with both anterior cingulate activation during performance on the
ANT in adults (Fan, Fossella, Sommer, Wu, & Posner, 2003) and disorganized attachment patterns in 12-
month-old infants (Lakatos et al., 2000). These findings point to potential gene–environment interactions
that impact on both cognitive and attachment organization relevant to BPD.
3.4. Implications for taxonomies of BPD and neighboring disorders
3.4.1. Co-occurring disorders

From the vantage point of the taxonomy of BPD, the high co-occurrence with other disorders,
heterogeneity, and absence of theoretically and psychometrically sound diagnostic thresholds suggests
that the current DSM nosology is not carving out borderline phenomena bat the jointsQ (Meehl, 1992). As
a way to account for co-occurring disorders, and to identify whether there is specificity of inhibition
impairment to diagnostic groups, Nigg (2000) and Korfine and Hooley (2000) recommend that more
than one type of inhibitory and memory process be studied concurrently across several disorders.
There are several frequently co-occurring disorders of particular relevance to BPD in the context of
cognition and memory, which could serve as optimal psychiatric comparison groups in future studies.
Antisocial personality and psychopathy are associated with executive cognitive control deficits, similar
to some of the findings we have reviewed in BPD (cf. Dolan & Park, 2002). Anxiety disorders and
3
A limitation of research on childhood abuse and neglect and BPD is a reliance on patient reports. Individuals with BPD (and others) may
exaggerate or minimize experiences of abuse and neglect for various reasons such as memory distortions, reluctance to be open with the
interviewer, amnesia, etc. Prospective, longitudinal studies of high-risk populations, starting in childhood, could best address this issue. Such an
approach would ideally rely on additional forms of evidence of abuse and neglect (e.g., medical records, police reports, and records from child
protective services). Such a study has not been conducted, to our knowledge.
depressive disorders are associated with affective cognitive and memory biases perhaps in some
similar and some contrasting ways compared to BPD (cf. Williams et al., 1996). Bipolar disorders are
characterized by mood instability and many have argued that BPD is a variant of the bipolar spectrum
disorders (cf. Deltito et al., 2001). One of the distinctions between the emotional dysregulation in
BPD vs. bipolar spectrum disorders may be the degree to which such dysregulations are sensitive to
socio-emotional and other environmental stimuli. Accordingly, experimental manipulation of such
stimuli when comparing BPD and bipolar subjects’ inhibitory and memory processing could begin to
address this distinction systematically. Affective memory biases, such as those found in BPD (Korfine
& Hooley, 2000) have been extensively documented in depressed individuals (see Mineka & Nugent,
1995 for review). Similar results have been obtained in individuals with Post Traumatic Stress
Disorder (PTSD). PTSD often co-occurs with BPD, and individuals with BPD have higher rates of
childhood and adult trauma and neglect than non-BPD individuals (Zanarini et al., 1997). For a fuller
consideration of the crucial area of diagnostic co-occurrence in BPD, and the role of neurobehavioral
studies in this area, we refer the reader to recent discussions of this issue (Lyons, Tyrer, Gunderson, &
Tohen, 1997).
3.5. Interface of neurocognition with clinical research, theory, and treatment of BPD
To the clinician who engages in the complex, often turbulent and challenging treatment of BPD,
executive neurocognition and memory systems may seem strikingly irrelevant to day-to-day therapeutic
challenges in this patient population. The pressing issues in the clinical engagement with individuals
with BPD include diagnostic confusion, suicidality and para-suicidality, complicated impasses,
enactments of interpersonal difficulties in the therapeutic relationship, and frequent interruptions and
drop-out from treatment. The following sections elaborate beginning connections that may forge
stronger links between the research cognition and memory and clinical practice with BPD.
3.5.1. Assessment
Increased understanding of the neurobehavioral facets of BPD should translate into more refined
diagnostic subtyping and, consequently, more targeted prevention and treatment initiatives for BPD. It
is reasonable to speculate that differing patterns of inhibitory and memory processes will respond
divergently to differing treatment approaches. In particular, the study of potential convergences
between phenomenological and neurocognitive domains would be a powerful paradigm for subtyping
BPD, with implications for differential treatment planning. Initial work in this area is promising. Using
a self-report adult temperament questionnaire developed by Rothbart, Posner and colleagues, BPD
subjects have been clustered into three subtypes based on the dimension of effortful control
(Hoermann, Clarkin, Levy, & Hull, 2005). The BPD cluster characterized by the lowest effortful
control exhibited the highest symptoms of depression, hostility, anxiety, and psychoticism, the most
social alienation, and the most difficulty with identity and reality testing. The converse was found for
the high effortful control sub-group, and the middle cluster was intermediate on most of these
dimensions.
With regard to the most life-threatening aspect of BPD, cognitive inhibition may to be a strong
predictor suicidality and parasuicidality. Keilp et al. (2001) compared three groups of subjects with
DSM-IV major depressive disorder (those without a history of suicide attempts, those with low lethality
suicide attempts, and those with high lethality suicide attempts), to non-patient control participants on
measures of attention, memory, and cognitive inhibition. They found that depressed subjects with prior
highly lethal suicide attempts had significantly greater deficits on cognitive inhibition compared to the
non-suicide depressed and normal subjects. By contrast, all depression subgroups were significantly
lower than the controls on measures of attention and memory. This finding seems consistent with a less
well-designed study (Burgess, 1991), which found that, within a BPD group, self-injurious behavior was
associated with neurocognitive impairment, but not with depression levels. These findings suggest that
deficits in executive neurocognition may be used to identify the highest risk BPD subjects, and intervene
accordingly to prevent suicidality and parasuicidality.
3.5.2. Treatment
Cognitive and memory impairments may improve during treatment. For instance, putative
hippocampal atrophy in relation to stress levels (McEwen, 1999) may be reversed by effective
psychopharmacologic and psychotherapeutic interventions, as the hippocampus exhibits much plasticity
throughout development. A parallel concept to stress reactivity, affect regulation, may also provide a
useful framework for linking BPD treatment with lab-based assessment of cognition and memory in
BPD. Affect regulation is defined as the deliberate and automatized procedures and individual uses to
enhance positive affects, and decrease negative and aversive emotions (cf. Dozier & Kobak, 1992; Perry
& Cooper, 1989). The deliberative aspects of affect regulation most likely involve the aspects of non-
affective constraint and effortful control systems. The automatized, non-voluntary aspects of affective
coping and regulatory strategies can be conceptualized as, in part, functions of procedural memory
(Bucci, 1997; Westen, 1994) that involve the automatized ways in which mental processes of attention,
self-appraisal, abstraction, and episodic memory recall increase or decrease affective reactions to internal
and external stimuli.
As both the temperament and attachment literature suggest, the quality of social bonds may
profoundly influence the development of memory systems and cognitive processing. The study of
social cognition (Westen, 1991) and adult attachment research (Fonagy, Target, Gergely, Allen, &
Bateman, 2003) are relevant paradigms in this arena. Preliminary assessment of aspects of social
cognition in adult BPD subjects indicate that they exhibit deficits in affect tone, complexity of
person perception, capacity for interpersonal investment, commitment to values and moral principles,
and self-understanding. Such deficits have been operationalized in the psychopathology and
psychodynamic literature as the quality of object relations (see Blatt, Auerbach, & Levy, 1997;
Hupricha & Greenberg, 2003, and Westen, 1991 for reviews). The object relations literature has
demonstrated that BPD individuals are vulnerable to experiencing interpersonal relationships as more
need gratifying, dangerous, and potentially exploitive than comparison groups. This literature has
also highlighted the difficulty BPD individuals have in interpreting ambiguous and complex social
stimuli, and in establishing accurate and unbiased causal attributions of interpersonal interactions.
Similarly, Fonagy et al. (1996) have demonstrated that traumatized BPD subjects can be
differentiated from other psychiatric subjects and matched control subjects by exhibiting lower
ratings on the capacity to be aware of the mental states of themselves and others. The extent to
which these social cognitive impairments are independent of or are mutually influential with
neurocognitive processes in BPD has not been studied, yet is crucial. Extrapolating these paradigms
to the study of the impact of psychotherapy on both social cognition and neurocognition in BPD
may provide exciting insights into the interplay between these two domains of information pro-
cessing during the treatment process.
4. Limitations and caveats
The studies of executive neurocognitive and memory processes and BPD share many
measurement and methodological limitations, and investigating BPD individuals raises many unique
challenges in clinical research, which we mention briefly. (1) The polythetic nature of DSM-IV
(American Psychiatric Association, 1994) BPD diagnostic system creates the frequent occurrence
that even individuals who meet criteria for BPD have quite different clinical presentations. (2) The
absence of empirically and prognostically meaningful diagnostic thresholds represents another
taxonomic and measurement issue. Widiger, Sanderson, and Warner (1986) found that those with
five BPD criteria, the minimum needed for the diagnosis, resemble non-DSM BPD individuals more
than BPD individuals. (3) Most of the studies reviewed demonstrated some attempt to assess non-
medicated BPD individuals, or to control for the effects of medication. In doing so, the trend was to
indicate in a binary manner whether a given participant was taking medication. However, few
studies indicated the class, dosage, number and type of different concurrent medications, and/or
length of medication use. There are more studies needed with subjects not on medication. (4) There
is considerable instability in the BPD diagnosis, and longitudinal studies indicate that both borderline
features (Lenzenweger, Johnson, & Willett, 2004; Stone, 1990, 1993; Zanarini, Frankenburg,
Hennen, & Silk, 2003) and neurocognitive performance (Kramer, Hahn, & Gopher, 1999; West,
1996) decrease significantly with age. While this may appear paradoxical, we speculate that
executive neurocognition may be less crucial as affective instability in BPD diminishes during
middle adulthood. However, only longitudinal studies of executive neurocognition and affective
instability and the course of BPD can assess this theory. (5) Most of the studies do not directly
address state/trait differentiation in cognition, memory, affect, and personality variables. This limits
the ecological validity of many of the studies, particularly since BPD is characterized in part by
rapidly shifting, context-sensitive affective states and cognitive appraisals. (6) Most studies utilized
either entirely female samples or predominantly female samples. This is consistent with the 3:1 ratio
of females to males found in clinically ascertained BPD samples (Corbitt & Widiger, 1995). Data on
male BPD subjects is particularly important given there is compelling evidence that gender
differences in BPD prevalence rates are only found in clinical settings (Corbitt & Widiger, 1995;
Torgersen et al., 2001). An earlier study suggested that gender differences in neurodevelopmental
history and clinical presentation were prominent in BPD (Andrulonis, Glueck, Stroebel, & Vogel,
1982). (7) Groups in the reviewed studies were not consistently matched on IQ and education level,
and these variables may underlie apparent group difference in executive neurocognition and memory
performance.
Finally, the association between executive neurocognition and impulsivity in BPD may simply reflect
an obvious tautology between the clinically rated diagnostic feature of impulsivity and its neurocognitive
correlates. If this was the case, there would be no additive advantage in using executive neurocognitive
assessment to reify the diagnostic features of BPD. This argument would, however, dismiss advantages
of a neurocognitive approach to research in BPD and impulsivity. Impulsivity appears to be a
multidimensional construct, with attentional, motor, and nonplanning subtypes (Patton, Stanford, &
Barratt, 1995). Executive neurocognitive tasks can contribute to parsing subtypes of impulsivity in
different psychiatric disorders. Neurocognitive measurement of constructs such as impulsivity can be
used to track changes over time and to decompose the sub-facets of such constructs. Also, the in-vivo
neurobiological correlates of impulsivity (such as 5HT synthesis; cf. Leyton et al., 2001) and
relationships to normal personality traits such as non-affective constraint (cf. Lenzenweger et al., 2004)
can then be both identified with lab based cognitive assessment.
5. Conclusion
In distillation, the main findings of this review are: (1) Well-characterized groups of BPD subjects
appear to exhibit non-specific deficits in multiple domains of executive neurocognitive and memory
performance in comparison to psychiatric and non-clinical groups. On a cautionary note, complicating
factors such as co-occurring conditions, state-dependent effects, omnibus measurement, small sample
sizes, and a limited number of studies implore us to be tentative about this pattern of findings. (2) Phase
III studies, while also limited in number and unreplicated, consistently suggest that motivational
influences and negative affects have a disorganizing and disruptive influence on executive
neurocognitive and memory performance in BPD compared to comparison groups.
There are a few observations regarding overall the state of investigation in executive neurocognition,
memory, and BPD, and promising areas for future investigation. First, it appears that the more emotional
stimuli are specifically tailored to the phenomenology of BPD the greater the impact on cognitive and
memory systems (e.g., Korfine & Hooley, 2000). Second, while there are associations between task
performance on certain cognitive and memory laboratory tasks and the diagnosis of BPD, very few
researchers have taken the next step and related the task performance to actual social behavior (e.g., social
behavior in dyadic relationships, suicidality, etc.). Additionally, longitudinal designs that assess the
stability and validity of associations between neurocognition, symptomatology, affectivity, and social
behavior are called for, given the emerging longitudinal data on the instability of the diagnosis, and the
rapidly shifting, state-dependent aspects of BPD.
As a final point, it could be argued that the main findings of the review are not surprising or
illuminating, as the notion that affects have a disorganizing effect on cognition and memory in BPD is
what clinicians have been describing for decades. While this is accurate, what is promising is that
clinically relevant phenomena can be rigorously operationalized and assessed in an experimental
laboratory context. The promise of the perspective of experimental psychopathology is that the features
and symptoms of devastating clinical phenomena–even multi-faceted and heterogeneous conditions like
BPD–can be assessed and related to basic biological and psychological mechanisms and systems
(Lenzenweger & Hooley, 2003). With collaboration and cross-fertilization, this translational effort should
eventually de-mystify and de-stigmatize this enigmatic disorder. Most importantly, firmer scientific
foundation in BPD research will inform more effective, research-based interventions. As a result, there is
compelling reason for hope that the devastating suffering that BPD causes to individuals and their families
can be mitigated as the neurobehavioral facets of the disorder are increasingly understood.
Acknowledgements
Preparation of this article was supported, in part, by the Leslie Glass Foundation, the Borderline
Personality Disorder Research Foundation, and an NIH National Research Service Award (MH015144).
We would like to thank John G. Keilp, Otto F. Kernberg, Michael I. Posner, Steven Roose, the
Research Group of the Columbia University Center for Psychoanalytic Training and Research, and three
anonymous reviewers for their thoughtful comments on earlier versions of this article. Melissa Stanley
provided helpful editorial assistance on this manuscript.
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Executive Neurocognition Memory Systems

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Clinical Psychology Review 26 (2006) 346 – 375

Executive neurocognition, memory systems,

1. Memory systems and cognitive inhibition: domains and methodologies

1.1. Memory systems

1.2. Executive neurocognition

2. Historical phases of cognitive inhibition and memory research on BPD

E.A. Fertuck et al. / Clinical Psychology Review 26 (2006) 346–375

Matched normal Yes No (compared BPD to ma- Yes Yes N/A

Working Memory Yes No Yes Yes Yes

- Immediate Repetition - WMS-R Associate

- (Corsi Blocks) - WMS-R

E.A. Fertuck et al. / Clinical Psychology Review 26 (2006) 346–375

Behavioral Inhibition / Yes Yes Yes Yes

IQ Not assessed Not assessed Yes Yes Yes

E.A. Fertuck et al. / Clinical Psychology Review 26 (2006) 346–375

E.A. Fertuck et al. / Clinical Psychology Review 26 (2006) 346–375

2.1. Phase I: phenomenological description of the BPD construct

E.A. Fertuck et al. / Clinical Psychology Review 26 (2006) 346–375

2.4. Executive neurocognition

2.4.1. Cognitive interference control

2.4.2. Cognitive inhibition/encoding

2.4.3. Behavioral inhibition

2.4.4. Motivational cognitive inhibition

2.4.5. Affective-cognitive inhibition

2.5. Memory systems

2.5.1. Autobiographical–episodic memory

2.6. Integrative summary of the three phases

Summary of Phase III findings:

1. Preliminary reports consistently point to impaired executive neurocognition in BPD, independent of

3.1. Neurobiological and neuroscience approaches

3.3. Developmental influences on executive neurocognition and memory in BPD

3.3.3. Adverse early experience

3.3.4. Attachment organization

3.4. Implications for taxonomies of BPD and neighboring disorders

3.4.1. Co-occurring disorders

4. Limitations and caveats

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